Pub Date : 2016-08-08DOI: 10.4172/2157-7412.1000300
A. Tajouri, Maryem M’sahli, S. Hizem, L. B. Jemaa, F. Maazoul, R. Mrad, H. Chaabouni, M. Kharrat
Mammalian sex is determined by a gene localized on the Y chromosome known as SRY (sex-determining region of the Y chromosome). SRY is a transcription factor that plays a key role in the initiation of the cascade of male sexual differentiation. In 46,XY humans, SRY mutations cause complete gonadal dysgenesis (CGD) with male to female sex reversal, which results in female genitalia without testis differentiation. The aim of this study was to look for mutations of SRY gene in a 46,XY CGD Tunisian female patient by direct sequencing. This method allowed us to identify a novel nonsense mutation L9X, occurring within the NH2 terminal domain of SRY. This novel mutation led to the appearance of a premature stop codon, resulting in a truncated protein, missing the entire HMG box functional domain and the COOH terminal domain. Because of an increased risk of developing gonadoblastoma, early molecular diagnosis allows the orientation of the clinical supervision by removing the dysgenetic gonads to prevent gonadal malignancy. Furthermore, it provides valuable information for the understanding of molecular mechanisms behind the gonadal dysgenesis.
{"title":"A Novel Nonsense Mutation p.L9X in the SRY Gene Causes Complete Gonadal Dysgenesis in a 46,XY Female Patient","authors":"A. Tajouri, Maryem M’sahli, S. Hizem, L. B. Jemaa, F. Maazoul, R. Mrad, H. Chaabouni, M. Kharrat","doi":"10.4172/2157-7412.1000300","DOIUrl":"https://doi.org/10.4172/2157-7412.1000300","url":null,"abstract":"Mammalian sex is determined by a gene localized on the Y chromosome known as SRY (sex-determining region of the Y chromosome). SRY is a transcription factor that plays a key role in the initiation of the cascade of male sexual differentiation. In 46,XY humans, SRY mutations cause complete gonadal dysgenesis (CGD) with male to female sex reversal, which results in female genitalia without testis differentiation. The aim of this study was to look for mutations of SRY gene in a 46,XY CGD Tunisian female patient by direct sequencing. This method allowed us to identify a novel nonsense mutation L9X, occurring within the NH2 terminal domain of SRY. This novel mutation led to the appearance of a premature stop codon, resulting in a truncated protein, missing the entire HMG box functional domain and the COOH terminal domain. Because of an increased risk of developing gonadoblastoma, early molecular diagnosis allows the orientation of the clinical supervision by removing the dysgenetic gonads to prevent gonadal malignancy. Furthermore, it provides valuable information for the understanding of molecular mechanisms behind the gonadal dysgenesis.","PeriodicalId":89584,"journal":{"name":"Journal of genetic syndromes & gene therapy","volume":"7 1","pages":"1-3"},"PeriodicalIF":0.0,"publicationDate":"2016-08-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"76963568","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2016-08-08DOI: 10.4172/2157-7412.1000302
Hongmei Ruan, M. Black
Acute myeloid leukemia (AML) is the most common type of acute leukemia. According to the National Cancer Institute, the new cases and deaths from AML in the United States in 2016 are estimated to be approximately 19,990 and 13,400, respectively, with a 5 year survival rate of only about 26.6% (http://seer.cancer.gov/statfacts/html/amyl. html). Thus, there is an urgent need to find more effective ways to improve the clinical treatment of AML.
{"title":"Zebularine-Resistant Human Cytidine Deaminase Mutants for Optimal Chemoprotection of Hematopoietic Stem Cells","authors":"Hongmei Ruan, M. Black","doi":"10.4172/2157-7412.1000302","DOIUrl":"https://doi.org/10.4172/2157-7412.1000302","url":null,"abstract":"Acute myeloid leukemia (AML) is the most common type of acute leukemia. According to the National Cancer Institute, the new cases and deaths from AML in the United States in 2016 are estimated to be approximately 19,990 and 13,400, respectively, with a 5 year survival rate of only about 26.6% (http://seer.cancer.gov/statfacts/html/amyl. html). Thus, there is an urgent need to find more effective ways to improve the clinical treatment of AML.","PeriodicalId":89584,"journal":{"name":"Journal of genetic syndromes & gene therapy","volume":"7 1","pages":"1-2"},"PeriodicalIF":0.0,"publicationDate":"2016-08-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"88701656","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2016-08-08DOI: 10.4172/2157-7412.1000301
D. Benharroch
We have suggested, several years ago, an association between the measles virus and classical Hodgkin lymphoma. However, this relationship was not accepted by the isolated research groups which dealt with the issue. In this short commentary, we recall the traits of the virus which were suggestive of a familiarity with Hodgkin lymphoma. We mention, in addition, older articles which highlight these similarities. As the impact of apoptosis in Hodgkin lymphoma is controversial, a chapter is saved for it. Atypical measles syndrome has long been forgotten. It is mentioned in the present context. The consensus agrees that immunity waning is not a significant factor regarding the measles virus. Is it indeed?
{"title":"The Measles Virus Expression Correlates with Classical Hodgkin Lymphoma and Other Malignancies. A Short Commentary","authors":"D. Benharroch","doi":"10.4172/2157-7412.1000301","DOIUrl":"https://doi.org/10.4172/2157-7412.1000301","url":null,"abstract":"We have suggested, several years ago, an association between the measles virus and classical Hodgkin lymphoma. However, this relationship was not accepted by the isolated research groups which dealt with the issue. In this short commentary, we recall the traits of the virus which were suggestive of a familiarity with Hodgkin lymphoma. We mention, in addition, older articles which highlight these similarities. As the impact of apoptosis in Hodgkin lymphoma is controversial, a chapter is saved for it. Atypical measles syndrome has long been forgotten. It is mentioned in the present context. The consensus agrees that immunity waning is not a significant factor regarding the measles virus. Is it indeed?","PeriodicalId":89584,"journal":{"name":"Journal of genetic syndromes & gene therapy","volume":"4 1","pages":"1-3"},"PeriodicalIF":0.0,"publicationDate":"2016-08-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"85352506","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2016-06-27DOI: 10.4172/2157-7412.1000299
N. Nørskov-Lauritsen, P. O. Schiøtz
CF is a progressive, lethal disease characterized by mucous build-up in the airways and a continuous annual deterioration of lung function. The host inflammatory response is considered a central pathological feature and constitutes an important target for non-steroidal anti-inflammatory drug therapy. Airway obstruction and bacterial colonization may cause inflammation, or it may be attributable to dysfunction of the cystic fibrosis transmembrane conductance regulator. Educational programs for this group of patients increase the compliance and quality-of-life, but cystic fibrosis patients have been recommended to abstain from attendance for concerns of microbial cross infection. When guidelines for optimal hand and respiratory hygiene and cough etiquette are observed in professionally supervised CF educational programs, an increased risk of bacterial transmission has not been documented. A recommendation to avoid indoor educational events with fellow CF patients must be weighed against the benefits of educational and rehabilitation programs. Further investigations are required to clarify the relative contribution of microbiological and genetic factors to the progression of CF lung disease.
{"title":"Transmission of Bacteria during Cystic Fibrosis Educational Programs","authors":"N. Nørskov-Lauritsen, P. O. Schiøtz","doi":"10.4172/2157-7412.1000299","DOIUrl":"https://doi.org/10.4172/2157-7412.1000299","url":null,"abstract":"CF is a progressive, lethal disease characterized by mucous build-up in the airways and a continuous annual deterioration of lung function. The host inflammatory response is considered a central pathological feature and constitutes an important target for non-steroidal anti-inflammatory drug therapy. Airway obstruction and bacterial colonization may cause inflammation, or it may be attributable to dysfunction of the cystic fibrosis transmembrane conductance regulator. Educational programs for this group of patients increase the compliance and quality-of-life, but cystic fibrosis patients have been recommended to abstain from attendance for concerns of microbial cross infection. When guidelines for optimal hand and respiratory hygiene and cough etiquette are observed in professionally supervised CF educational programs, an increased risk of bacterial transmission has not been documented. A recommendation to avoid indoor educational events with fellow CF patients must be weighed against the benefits of educational and rehabilitation programs. Further investigations are required to clarify the relative contribution of microbiological and genetic factors to the progression of CF lung disease.","PeriodicalId":89584,"journal":{"name":"Journal of genetic syndromes & gene therapy","volume":" 23","pages":"1-4"},"PeriodicalIF":0.0,"publicationDate":"2016-06-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"72381154","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2016-06-08DOI: 10.4172/2157-7412.1000298
Mohamed S. A. Mohamed
While the genetic matching between the donor and the recipient is essential for the success of the transplant procedure, there are other genetic factors that have the potential to significantly influence the clinical outcome. In this paper, the light is shed on this notion from a relatively new point of view.
{"title":"Role of Genetic Testing in Lung Transplantation; Prediction of Inflammation","authors":"Mohamed S. A. Mohamed","doi":"10.4172/2157-7412.1000298","DOIUrl":"https://doi.org/10.4172/2157-7412.1000298","url":null,"abstract":"While the genetic matching between the donor and the recipient is essential for the success of the transplant procedure, there are other genetic factors that have the potential to significantly influence the clinical outcome. In this paper, the light is shed on this notion from a relatively new point of view.","PeriodicalId":89584,"journal":{"name":"Journal of genetic syndromes & gene therapy","volume":"22 1","pages":"1-3"},"PeriodicalIF":0.0,"publicationDate":"2016-06-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"73448750","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2016-05-20DOI: 10.4172/2157-7412.1000297
I. Gómez-Manjón, A. Moreno-Izquierdo, M. Moreno-García, D. Escribano, F. J. Fernández-Martínez
Massively parallel sequencing of cell free fetal DNA (cffDNA) obtained from maternal plasma is used to detect fetal trisomies and selected sex chromosomal aneuploidies. Different technologies can be used to detect fetal chromosomopathies noninvasively, such as Next Generation sequencing and microarrays. In this case report, we show a procedure for detecting chromosomal imbalances as a result of balanced translocations inherited from parents, using noninvasive prenatal detection of common aneuploidies based protocol. This case study illustrates the potential power of whole-genome semiconductor sequencing when used to augment the diagnostic spectrum of noninvasive prenatal testing to detection of copy number variants.
{"title":"Noninvasive Prenatal Detection of a Partial Trisomy 4 Using Whole Genome Semiconductor Sequencing","authors":"I. Gómez-Manjón, A. Moreno-Izquierdo, M. Moreno-García, D. Escribano, F. J. Fernández-Martínez","doi":"10.4172/2157-7412.1000297","DOIUrl":"https://doi.org/10.4172/2157-7412.1000297","url":null,"abstract":"Massively parallel sequencing of cell free fetal DNA (cffDNA) obtained from maternal plasma is used to detect fetal trisomies and selected sex chromosomal aneuploidies. Different technologies can be used to detect fetal chromosomopathies noninvasively, such as Next Generation sequencing and microarrays. In this case report, we show a procedure for detecting chromosomal imbalances as a result of balanced translocations inherited from parents, using noninvasive prenatal detection of common aneuploidies based protocol. This case study illustrates the potential power of whole-genome semiconductor sequencing when used to augment the diagnostic spectrum of noninvasive prenatal testing to detection of copy number variants.","PeriodicalId":89584,"journal":{"name":"Journal of genetic syndromes & gene therapy","volume":"137 1","pages":"1-4"},"PeriodicalIF":0.0,"publicationDate":"2016-05-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"86283194","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2016-05-17DOI: 10.4172/2157-7412.1000295
T. M. Malla, M. Zargar, F. Dar, Z. Shah
Clastogen induced chromosome breakage analysis is widely used for the differential diagnosis of Fanconi's anemia. Mitomycin-C (MMC) induced chromosome fragility test was performed on the cultured lymphocytes of 50 children with clinical suspicion of Fanconi's anemia. According to the results of the MMC test, the patients were divided into two subgroups: FA displaying typical sensitivity to MMC and non FA. The present study revealed 7(14%) of examined patients to have a FA cellular phenotype with increased MMC-induced chromosome fragility. The percentage of MMC-induced aberrant cells was increased more than 36 times in FA patients (Mean=67.14%) when compared to non FA patients (Mean=1.82). The number of MMC-induced breaks/cells was more than 09 times higher in FA patients (Mean=2.42 breaks/cell) when compared to non FA patients (Mean=0.25 breaks/cells). Our results indicate that the clastogen induced sensitivity test is a reliable in vitro method for verification of the FA cellular phenotype. The study being the first of its kind from Kashmir (North India) lays the basis for further studies on patients of this region with a clinical suspicion of FA.
{"title":"Clastogen-Induced Chromosomal Breakage Analysis of Suspected Fanconis Anemia Cases of Kashmir, North India","authors":"T. M. Malla, M. Zargar, F. Dar, Z. Shah","doi":"10.4172/2157-7412.1000295","DOIUrl":"https://doi.org/10.4172/2157-7412.1000295","url":null,"abstract":"Clastogen induced chromosome breakage analysis is widely used for the differential diagnosis of Fanconi's anemia. Mitomycin-C (MMC) induced chromosome fragility test was performed on the cultured lymphocytes of 50 children with clinical suspicion of Fanconi's anemia. According to the results of the MMC test, the patients were divided into two subgroups: FA displaying typical sensitivity to MMC and non FA. The present study revealed 7(14%) of examined patients to have a FA cellular phenotype with increased MMC-induced chromosome fragility. The percentage of MMC-induced aberrant cells was increased more than 36 times in FA patients (Mean=67.14%) when compared to non FA patients (Mean=1.82). The number of MMC-induced breaks/cells was more than 09 times higher in FA patients (Mean=2.42 breaks/cell) when compared to non FA patients (Mean=0.25 breaks/cells). Our results indicate that the clastogen induced sensitivity test is a reliable in vitro method for verification of the FA cellular phenotype. The study being the first of its kind from Kashmir (North India) lays the basis for further studies on patients of this region with a clinical suspicion of FA.","PeriodicalId":89584,"journal":{"name":"Journal of genetic syndromes & gene therapy","volume":"17 1","pages":"1-4"},"PeriodicalIF":0.0,"publicationDate":"2016-05-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"82878656","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2016-05-17DOI: 10.4172/2157-7412.1000296
S. Asadi, Ali Nazirzadeh, Elnaz Heydari, Saeedeh Habibi
Syndrome Raine, a severe skeletal dysplasia is usually caused the deaths of patients aged newborn. There are reports that patients with a milder form of the disease to live longer and have reached the age of a child. Radiological surveys show an increase in bone density generalized sclerosis and osteoarthritis. Bone density at the base of the skull, causing changes in the craniofacial skeleton, leading to specific dysmorphic signs in the figures. Symptoms of the disease include prominent forehead, proptosis, nasal root sunk, hypoplastic middle part of the face, hypoplastic nose, mouth, triangular, Atresia Cowan and intracranial calcification. Bone density in the disease so that the disease osteopetrosis is wrong. Raine syndrome is an autosomal recessive hereditary disease, which is caused by mutations in the gene is FAM20C. This gene encodes a protein that phosphorylase-kinase activity has been implicated in bio-mineralization. In this study, a patient with Raine syndrome is introduced from Iran. Based on available information, this patient is the first known case in Iran reported. Molecular analysis of the patient, a homozygous mutation new were identified. Already known about the patient's seventeenth in the world.
{"title":"Syndrome Raine, A Rare Autosomal Recessive Dysplasia Sclerotic Osteoarthritis, the First Reports of a New Mutation of Tabriz City in IRAN","authors":"S. Asadi, Ali Nazirzadeh, Elnaz Heydari, Saeedeh Habibi","doi":"10.4172/2157-7412.1000296","DOIUrl":"https://doi.org/10.4172/2157-7412.1000296","url":null,"abstract":"Syndrome Raine, a severe skeletal dysplasia is usually caused the deaths of patients aged newborn. There are reports that patients with a milder form of the disease to live longer and have reached the age of a child. Radiological surveys show an increase in bone density generalized sclerosis and osteoarthritis. Bone density at the base of the skull, causing changes in the craniofacial skeleton, leading to specific dysmorphic signs in the figures. Symptoms of the disease include prominent forehead, proptosis, nasal root sunk, hypoplastic middle part of the face, hypoplastic nose, mouth, triangular, Atresia Cowan and intracranial calcification. Bone density in the disease so that the disease osteopetrosis is wrong. Raine syndrome is an autosomal recessive hereditary disease, which is caused by mutations in the gene is FAM20C. This gene encodes a protein that phosphorylase-kinase activity has been implicated in bio-mineralization. In this study, a patient with Raine syndrome is introduced from Iran. Based on available information, this patient is the first known case in Iran reported. Molecular analysis of the patient, a homozygous mutation new were identified. Already known about the patient's seventeenth in the world.","PeriodicalId":89584,"journal":{"name":"Journal of genetic syndromes & gene therapy","volume":"41 1","pages":"1-6"},"PeriodicalIF":0.0,"publicationDate":"2016-05-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"76796468","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2016-05-05DOI: 10.4172/2157-7412.1000294
T. Szabó, A. Ujfalusi, B. Bessenyei, G. Szabó, K. Szakszon, I. Balogh, É. Oláh
15q11-13 chromosome region contains five breakpoints (BP1-BP5). Chromosomal rearrangements are common in this region. The microdeletion of BP1-BP2 region represents the 15q11.2 microdeletion syndrome associating with variable phenotype. We investigated a ten years old boy with hypotony. His motoric functions, speech and intellectual development were delayed. He suffered from epilepsy and showed dysmorphic features. Some of these dysmorphic features such us epicanthus and the clynodactyly of the fifth fingers can be observed in Angelman or Prader-Willi syndromes but have not been described in the 15q11.2 microdeletion syndrome so far. He has congenital torticollis that has been described earlier neither in this microdeletion syndrome nor in Prader-Willi - Angelman syndromes. Our aim is to find the possible mechanisms leading to the phenotype using Metilation Specific - Multi Ligand Probe Assay, Polimerase Chain Reaction and Array Comparative Genomic Hybridization. The 15q11.2 microdeletion syndrome represents an example for the incomplete penetrance and variable expressivity. Further genetic changes, such as other defective genes, further copy number variations, variability in non-coding regions, the mRNA quantity, environmental effects and epigenetic modification may also influence on the severity of the symptoms. We suggest to classify the symptoms into two groups (major and minor criteria). Depending on the existing minor criteria, this syndrome could be identified as Angelman-like or Prader-Willi-like syndromes.
{"title":"Torticollis in 15q11.2 Microdeletion Syndrome: a Rare Association in Angelman-like Syndromes","authors":"T. Szabó, A. Ujfalusi, B. Bessenyei, G. Szabó, K. Szakszon, I. Balogh, É. Oláh","doi":"10.4172/2157-7412.1000294","DOIUrl":"https://doi.org/10.4172/2157-7412.1000294","url":null,"abstract":"15q11-13 chromosome region contains five breakpoints (BP1-BP5). Chromosomal rearrangements are common in this region. The microdeletion of BP1-BP2 region represents the 15q11.2 microdeletion syndrome associating with variable phenotype. We investigated a ten years old boy with hypotony. His motoric functions, speech and intellectual development were delayed. He suffered from epilepsy and showed dysmorphic features. Some of these dysmorphic features such us epicanthus and the clynodactyly of the fifth fingers can be observed in Angelman or Prader-Willi syndromes but have not been described in the 15q11.2 microdeletion syndrome so far. He has congenital torticollis that has been described earlier neither in this microdeletion syndrome nor in Prader-Willi - Angelman syndromes. Our aim is to find the possible mechanisms leading to the phenotype using Metilation Specific - Multi Ligand Probe Assay, Polimerase Chain Reaction and Array Comparative Genomic Hybridization. The 15q11.2 microdeletion syndrome represents an example for the incomplete penetrance and variable expressivity. Further genetic changes, such as other defective genes, further copy number variations, variability in non-coding regions, the mRNA quantity, environmental effects and epigenetic modification may also influence on the severity of the symptoms. We suggest to classify the symptoms into two groups (major and minor criteria). Depending on the existing minor criteria, this syndrome could be identified as Angelman-like or Prader-Willi-like syndromes.","PeriodicalId":89584,"journal":{"name":"Journal of genetic syndromes & gene therapy","volume":"27 1","pages":"1-5"},"PeriodicalIF":0.0,"publicationDate":"2016-05-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"75336719","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2016-04-15DOI: 10.4172/2157-7412.1000293
S. Arumugam, Jayandharan Gr
Figure 1: Schematic representation of AAV genome in Arthrobacter sp. LS16 annotated sequence (3736126-3743962): The 7837nt region (B) consisting R1-Arthrobacter Repeat region 1, GLYCA-partial human alpha glycoprotein hormone gene, MCS-multiple cloning site, PA-simian virus 40 poly A tail, ΔE1-partial adeno viral early protein intron, Adeno-associated virus replication and capsid gene, ORI-E.coli origin of replication, KAN-kanamycin resistance gene, LITR-left inverted terminal repeat of AAV, CMVP-cytomegalovirus promoter and R2-Arthrobacter Repeat region 2 are shown.
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